In the past, atrial arrhythmias have been largely undertreated due to the perception that these arrhythmias are relatively benign. As more serious consequences of persistent atrial fibrillation have come to be understood, such as an associated risk of relatively more serious ventricular arrhythmias and stroke, there is a greater interest in providing implantable atrial or dual chamber cardioverter defibrillators for treating atrial arrhythmias.
Atrial arrhythmias, including atrial tachycardia (AT) and atrial fibrillation (AF) may be treated by either anti-tachycardia pacing therapies or high-voltage cardioversion/defibrillation shocks, or both. The high-voltage cardioversion/defibrillation shocks can be very painful to the patient. Since anti-tachycardia pacing (ATP) therapies are typically not perceived by the patient and generally consume less battery charge than high-voltage therapies, ATP therapies are typically attempted first in terminating an atrial arrhythmia. If the first ATP therapy delivered is not successful in terminating the atrial arrhythmia, a sequence of ATP therapies may be attempted. Since atrial arrhythmias are not directly life-threatening, delays in converting an atrial arrhythmia due to failed ATP therapies is tolerable. ATP therapies generally employ high rate pacing pulses or pulse bursts in an attempt to “overdrive” pace the heart such that re-entrant pathways sustaining an arrhythmia are interrupted.
Anti-tachycardia pacemakers are generally disclosed in U.S. Pat. No. 4,511,633 issued to Berkovits et al., U.S. Pat. No. 4,587,970 issued to Holley et al., U.S. Pat. No. 4,880,005 issued to Pless et al., and U.S. Pat. No. 4,726,380 issued to Vollmann et al., and U.S. Pat. No. 6,400,986 issued to Sun et al. Systems for delivering anti-tachycardia pacing pulses for treating atrial fibrillation are generally disclosed in PCT Publication No. WO95/28988 issued to Mongeon et al., and in PCT Publication No. WO95/28987 issued to Combs et al.
One risk associated with delivering atrial ATP therapies is that ventricular arrhythmias may be induced during or soon after ATP delivery. This pro-arrhythmic effect of atrial ATP therapies on the ventricle occurs when atrial pacing pulses are rapidly conducted to the ventricles thereby inducing ventricular arrhythmia. Ventricular pro-arrhythmia due to atrial ATP may also occur if the atrial pacing pulses capture the ventricular tissue inadvertently, due to a poorly placed or dislodged atrial pacing lead. It is highly undesirable to induce a more serious ventricular arrhythmia in the process of treating a less serious atrial arrhythmia. Typically, if a ventricular arrhythmia, including ventricular tachycardia or ventricular fibrillation, is detected immediately following an ATP therapy, the atrial arrhythmia therapies are disabled, even if the atrial arrhythmia is still present, so that the more serious ventricular arrhythmia can be treated.
Currently, ICDs control arrhythmia therapy delivery based on the type of arrhythmia detected independent of the rhythm of the opposite chamber. Detection of ventricular arrhythmias generally takes precedence over the detection of atrial arrhythmias because of the more serious nature of ventricular arrhythmias. Reference is made, for example, to U.S. Pat. No. 5,545,186 issued to Olson et al., which generally discloses a prioritized rule-based algorithm for arrhythmia detection, incorporated herein by reference in its entirety. Such prioritized arrhythmia detection has important advantages in detecting and treating the most lethal forms of arrhythmias first. For example, once a ventricular arrhythmia has been diagnosed by review of both atrial and ventricular information, therapies are delivered for treatment of the ventricular arrhythmia independent of the atrial rhythm at the time. If, however, an atrial arrhythmia is detected and an atrial ATP therapy is needed, the ATP therapy is delivered independent of the ventricular rhythm unless a ventricular arrhythmia is detected subsequent to an ATP therapy.
From the above discussion, however, it is apparent that it is desirable to avoid the ventricular pro-arrhythmic effects when delivering atrial ATP therapies. A need remains, therefore, for a method for controlling the delivery of atrial ATP therapies that includes monitoring the ventricular rhythm for pro-arrhythmic effects. Such a method preferably allows atrial ATP therapies to be disabled or aborted when ventricular pro-arrhythmia is evident in order to avoid inducing a ventricular arrhythmia as a result of treating an atrial arrhythmia.